Catálogo de publicaciones - libros

In recent years, investigators have used a variety of techniques to study human neurotransmission in health and disease. One of the most promising of these techniques is molecular or neurotransmitter imaging, which, despite being an emerging technique, has made significant contribution to our understanding of human neurotransmission (1,2). Molecular imaging has been used by numerous investigators to establish maps of the functional anatomy of neuroreceptorradioligand interaction (3,4). Recently, it has been applied to the detection of dynamic changes in neurotransmitter activity induced by behavioral, cognitive, or pharmacologic interventions (5-12). This chapter includes a brief outline of the basic concepts of neurotransmitter imaging, important information acquired using this technique, and a discussion of dynamic receptor imaging.

An improved understanding of the pathophysiology of myocardial ischemia combined with the development of new diagnostic modalities has substantially modified the concepts of myocardial blood flow (MBF) and left ventricular function in coronary artery disease (CAD). Positron emission tomography (PET) has emerged as a unique tool to characterize physiologic and pathologic processes, and it already plays a significant role in different areas of clinical medicine, including cardiology. Cardiac PET is based on the properties of positron emitters and radiation detection to provide a noninvasive and in vivo assessment of regional myocardial perfusion and metabolism. Different study protocols have been largely used in the adult population to detect and grade the severity of coronary artery disease during the last two decades using cardiac PET technology. Further, cardiac PET using fluorine-18 (18F) 2-fluoro-2-deoxyglucose (FDG) is considered the gold standard imaging modality for the assessment of myocardial viability (1) and is well recognized as providing accurate information on the long-term prognosis of the patients with chronic coronary ischemic disease (2).

The original criteria for fever of unknown origin (FUO) as set forth in 1961 by Petersdorf and Beeson were fever higher than 38.3°C on several occasions of at least 3 weeks’ duration and uncertain diagnosis after 1 week of study in the hospital (1). This definition was later revised, and the criterion of 1 week of hospitalization has been replaced by 3 days of hospitalization or three outpatient visits (2,3). In addition to the previously described classic FUO, additional categories have been added: nosocomial, neutropenic, and HIV-associated FUO (3,4).

Positron emission tomography (PET) with fluorine-18 (18F)-fluoro-2-deoxyglucose (FDG) has been proven to be a valuable noninvasive imaging modality for the diagnosis, staging, and monitoring of therapy for various malignancies. In addition, studies are demonstrating the value of FDG-PET for the evaluation of nononcologic conditions. Based on the literature, conditions such as osteomyelitis, fever of unknown origin (FUO), acquired immunodeficiency syndrome (AIDS), vasculitis, and inflammatory bowel disease can be successfully imaged with FDG-PET. With the approval of additional PET radiotracers in the future, there will be more widespread applications of PET for inflammatory and infectious disorders.

In the 1970s, research with positron emission tomography (PET) expanded in the fields of cardiology and neurology, but since the 1990s a dramatic upsurge of PET occurred in oncology applications using mostly fluorodeoxyglucose (FDG). This development can be explained by the ability to obtain whole-body acquisition and good image quality and by an improvement of the availability of FDG. However, FDG is not tumor specific. False-positive FDG-PET results in cases of infection and inflammation are well known (1,2). The first report of PET use in infection was the description of FDG uptake in abdominal abscesses in 1989 (3). This led some to consider PET with FDG as a useful tool for rapid detection of infectious processes (4). This property was considered as an opportunity to use FDG-PET in the diagnosis and followup of infectious or inflammatory processes, where it can replace other investigations, for instance, using white blood cell scintigraphy as well as Ga-67.

Hyperinsulinism (HI) is the most important cause of recurrent hypoglycemia in infancy. The hypersecretion of insulin induces profound hypoglycemias that require aggressive treatment to prevent the high risk of neurologic complications (1,2). Hyperinsulinism can be due to two different histopathologic types of lesions, a focal or a diffuse form (3,4), based on different molecular entities despite an indistinguishable clinical pattern (5-9). In focal HI, which represents about 40% of all cases (10), the pathologic pancreatic b cells are gathered in a focal adenoma, usually 2.5 to 7.5mm in diameter. Conversely, diffuse HI corresponds to an abnormal insulin secretion of the whole pancreas with disseminated b cells showing enlarged abnormal nuclei (11). Finally, about 10% of HI cases are clinically atypical and could not be classified, having unknown molecular basis and histopathologic form (12).

Congenital hyperinsulinism is the most common cause of persistent hypoglycemia in infants and children (1). Infants with severe forms of the disorder (formerly termed nesidioblastosis) present with hypoglycemia in the newborn period and are at high risk of seizures, permanent brain damage, and retardation. Infants with congenital hyperinsulinism may have either focal or diffuse abnormalities of the pancreatic β cells. In cases with diffuse disease, an underlying defect in the β-cell adenosoine triphosphate (ATP)-dependent potassium channel may be present, caused by recessive loss of function mutations of the two genes encoding the KATP channel, SUR1 or Kir6.2 (1,2). These mutations may also cause focal hyperinsulinism in which there is an area of β-cell adenomatosis due to loss of heterozygosity for the maternal 11p region and expression of a paternally derived KATP channel mutation (3). Most of the cases with severe hyperinsulinism do not respond to medical therapy with diazoxide, octreotide (Fig. 27B.1), or continuous feedings and require near-total pancreatectomy to control hypoglycemia. However, cases of focal hyperinsulinism can be treated effectively with partial pancreatectomy. The surgical approach and therapeutic outcome for the infants depends on preoperatively distinguishing between focal and diffuse forms of hyperinsulinism. This chapter describes the focal lesions of hyperinsulinism, the pancreatectomy procedure, previous methods of determining the site of focal lesions, and the rationale for using positron emission tomography (PET) scans with ^18F-fluoro-L-DOPA.

Magnetic resonance imaging (MRI) and positron emission tomography (PET) are diagnostic imaging modalities that facilitate visualization of morphologic as well as functional features of different diseases in childhood. Both modalities are often used separately or even in competition. Some of the most important indications for both PET and MRI lie in the field of pediatric oncology. The malignant diseases in children are leukemia, brain tumors, lymphomas, neuroblastoma, soft tissue sarcomas, Wilms’ tumor, and bone sarcomas. Apart from leukemia, correct assessment of tumor expansion with modern imaging techniques, mainly consisting of ultrasonography, computed tomography (CT), MRI, and PET, is essential for cancer staging, for the choice of the best therapeutic approach, and for restaging after therapy or in recurrence (1,2).

Over the past 20 years, as clinical applications have been gradually expanding, positron emission tomography (PET) has become an indispensable imaging technique in several medical fields such as oncology, neurology, and cardiology. Application of PET in pediatrics is still very limited, likely due to the smaller number of clinical reports involving PET in pediatric as compared to adult medicine and to the lesser availability of PET scanners in pediatric facilities. However, the recent expansion of the regional availability of the most common PET radiotracer, fluorine-18 fluorodeoxyglucose (^18F-FDG) and, more importantly, the recent appearance of the dual-modality PET-computed tomography(CT) imaging system have provided new opportunities of expansion of PET to the pediatric field. The recent mechanical coupling of CT to PET in the same imaging device for attenuation correction permits precise localization of metabolic findings on anatomic images and shortens the total acquisition time. Both qualities are particularly important in pediatric imaging, making the study more acceptable to patients and parents and less cumbersome for personnel. Moreover, the shortened acquisition time reduces the probability of motion artifacts on reconstructed images. This chapter briefly summarizes the state of clinical applications of PET in the pediatric field and discusses potential new research approaches and new clinical applications of PET and PET-CT in pediatric patients.

Fluorine-18-fluorodeoxyglucose (FDG) positron emission tomography (PET) is a functional imaging modality that capitalizes on the fact that pathologic processes are generally highly metabolically active and accumulate more glucose (and FDG) than normal tissue. However, sites of normal metabolic activity can also demonstrate intense FDG uptake and can sometimes be difficult to distinguish from disease activity. Fusion imaging modalities that acquire both functional and correlative anatomic imaging provide an important advantage over PET alone because they allow the accurate anatomic localization of sites of increased FDG activity (1–5). In this chapter, normal sites of FDG activity are correlated with computed tomography (CT) anatomy in images obtained during PET-CT scanning. Examples of pathologic FDG activity are included to illustrate the unique value of this fusion imaging modality in distinguishing normal from pathologic activity.